Although verapamil, the prototype calcium channel blocking agent, has been shown to have hemodynamic effects which should be of benefit to patients with hypertrophic cardiomyopathy, our studies with nifedipine, another calcium channel blocking drug, have not shown consistent beneficial effects. A gas chromatographic assay was used to measure blood nifedipine levels, which were then correlated with the hemodynamic effects. Nifedipine levels plateaued 20 minutes after the administration of either 10 or 20 mg buccally and did not significantly increase even with the administration of a second 10 mg dose. The values were similar, independent of whether 10 or 20 mg was administered as the first dose. As expected, there was a linear relationship between nifedipine concentrations and increases in heart rate and decreases in peripheral vascular resistance. Cardiac output increased only as a result of heart rate changes. Pulmonary wedge pressure was also linearly related to nifedipine levels. In contrast to our results with verapamil administration, left ventricular outflow tract obstruction was not affected at lower nifedipine levels (Less than 80ng/ml), but actually increased (14plus or minus26%, p Less than 0.05) at levels above this concentration. Also different from the verapamil findings was the fact that nifedipine had no effect on indicators of systolic and diastolic left ventricular function. Thus we were not able to demonstrate any beneficial hemodynamic effects of buccally administered nifedipine to patients with hypertrophic cardiomyopathy. Moreover, at higher concentrations of the drug, there was a tendency for detrimental effects to occur, a reduction in stroke volume, and increase in left ventricular outflow tract obstruction, and an elevation of left ventricular filling pressures.